New research from the University of North Carolina at Chapel Hill School of Medicine adds clarity to the connection. The study published on-line April 10th in the journal Nature Immunology finds that saturated fatty acids but not the unsaturated type can activate immune cells to produce an inflammatory protein, called interleukin-1beta.

CHAPEL HILL, N.C. – A diet high in saturated fat is a key contributor to type 2 diabetes, a major health threat worldwide. Several decades ago scientists noticed that people with type 2 diabetes have overly active immune responses, leaving their bodies rife with inflammatory chemicals.

In addition, people who acquire the disease are typically obese and are resistant to insulin, the hormone that removes sugar from the blood and stores it as energy.

For years no one has known exactly how the three characteristics are related. But a handful of studies suggest that they are inextricably linked.

“The cellular path that mediates fatty acid metabolism is also the one that causes interleukin-1beta production,” says senior study co-author Jenny Y. Ting, PhD, William Kenan Rand Professor in the Department of Microbiology and Immunology.

“Interleukin-1beta then acts on tissues and organs such as the liver, muscle and fat (adipose) to turn off their response to insulin, making them insulin resistant. As a result, activation of this pathway by fatty acid can lead to insulin resistance and type 2 diabetes symptoms.” Ting is also a member of the UNC Lineberger Comprehensive Cancer Center, and the UNC Inflammatory Diseases Institute.

Other authors of the report, all in the Department of Microbiology and Immunology, are postdoctoral researcher and first author Haitao Wen, Denis Gris, Yu Lei, Shushmita Jha; Lu Zhang, Max Tze-Han Huang, and Willie June Brickey.

The research was supported in part by the National Institutes of Health and the American Heart Association Mid-Atlantic Affiliate.